The role of decorin in cardiovascular diseases: more than just a decoration

Vu, Thu Thi; Marquez, Jubert; Long, Lê Thanh; Nguyen, Anh; Kim, Hyoung Kyu; Han, Jin

doi:10.1080/10715762.2018.1516285

Cited by 26 publications

(16 citation statements)

References 88 publications

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“…For example, DCN interacts with TGF-β, a major activator of fibrinogenesis, to suppress its response. The reduced TGF-β reception can further mitigate inflammation, fibrosis and tissue hypoxia in the context of metabolic disorders such as obesity and non-alcoholic steatohepatitis (NASH) (145).…”

Section: Decorin -Friend or A Foe In Inflammatory Diseases?mentioning

confidence: 99%

Proteoglycans in Obesity-Associated Metabolic Dysfunction and Meta-Inflammation

2020

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Proteoglycans are a specific subset of glycoproteins found at the cell surface and in the extracellular matrix, where they interact with a plethora of proteins involved in metabolic homeostasis and meta-inflammation. Over the last decade, new insights have emerged on the mechanism and biological significance of these interactions in the context of diet-induced disorders such as obesity and type-2 diabetes. Complications of energy metabolism drive most diet-induced metabolic disorders, which results in low-grade chronic inflammation, thereby affecting proper function of many vital organs involved in energy homeostasis, such as the brain, liver, kidney, heart and adipose tissue. Here, we discuss how heparan, chondroitin and keratan sulfate proteoglycans modulate obesityinduced metabolic dysfunction and low-grade inflammation that impact the initiation and progression of obesity-associated morbidities.

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Section: Decorin -Friend or A Foe In Inflammatory Diseases?mentioning

confidence: 99%

Proteoglycans in Obesity-Associated Metabolic Dysfunction and Meta-Inflammation

2020

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“…Moreover, the collagen binding protein dcn and Aspn both were increased. dcn is a proteoglycan constituent of the EcM reported to possess powerful anti-inflammation properties in cardiovascular diseases (69). These results suggested that a possible degradation of the collagen component in EcM of the spinal cord and the collagen metabolism may be involved in the regulation in the spinal cord in response to myocardial IR injury in rats.…”

Section: Discussionmentioning

confidence: 85%

Quantitative proteomics reveal the alterations in the spinal�cord after myocardial ischemia‑reperfusion injury in rats

et al. 2019

Int J Mol Med

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There is now substantial evidence that myocardial ischemia-reperfusion (IR) injury affects the spinal cord and brain, and that interactions may exist between these two systems. In the present study, the spinal cord proteomes were systematically analyzed after myocardial IR injury, in an attempt to identify the proteins involved in the processes. The myocardial IR injury rat model was first established by cross clamping the left anterior descending coronary artery for 30-min ischemia, followed by reperfusion for 2 h, which resulted in a significant histopathological and functional myocardial injury. Then using the stable isotope dimethyl labeling quantitative proteomics strategy, a total of 2,362 shared proteins with a good distribution and correlation were successfully quantified. Among these proteins, 33 were identified which were upregulated and 57 were downregulated in the spinal cord after myocardial IR injury, which were involved in various biological processes, molecular function and cellular components. Based on these proteins, the spinal cord protein interaction network regulated by IR injury, including apop-tosis, microtubule dynamics, stress-activated signaling and cellular metabolism was established. These heart-spinal cord interactions help explain the apparent randomness of cardiac events and provide new insights into future novel therapies to prevent myocardial I/R injury.

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“…Note also that decreased autophagy is involved in the pathogenesis of inflammaging, fibrotic diseases and tumors. Studies have shown a reduction of decorin in different fibrotic organs, as in cardiac fibrosis following myocardial infarction and in acute exacerbation-idiopathic pulmonary fibrosis (IPF) (70)(71)(72). Animal experiments in decorin-null mice with myocardial infarction (70) or in hamster and mice models of lung fibrosis (73-75) showed both decorin requirement for proper fibrotic evolution of tissue injury and the potential therapeutic antifibrotic effect of decorin administration.…”

Section: Granzyme B: Epithelial-to-mesenchymal Transition and Fibrosimentioning

confidence: 99%

Granzyme B in Inflammatory Diseases: Apoptosis, Inflammation, Extracellular Matrix Remodeling, Epithelial-to-Mesenchymal Transition and Fibrosis

et al. 2020

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Inflammation is strictly interconnected to anti-inflammatory mechanisms to maintain tissue homeostasis. The disruption of immune homeostasis can lead to acute and chronic inflammatory diseases, as cardiovascular, pulmonary, metabolic diseases and cancer. The knowledge of the mechanisms involved in the development and progression of these pathological conditions is important to find effective therapies. Granzyme B (GrB) is a serine protease produced by a variety of immune, non-immune and tumor cells. Apoptotic intracellular and multiple extracellular functions of GrB have been recently identified. Its capability of cleaving extracellular matrix (ECM) components, cytokines, cell receptors and clotting proteins, revealed GrB as a potential multifunctional pro-inflammatory molecule with the capability of contributing to the pathogenesis of different inflammatory conditions, including inflammaging, acute and chronic inflammatory diseases and cancer. Here we give an overview of recent data concerning GrB activity on multiple targets, potentially allowing this enzyme to regulate a wide range of crucial biological processes that play a role in the development, progression and/or severity of inflammatory diseases. We focus our attention on the promotion by GrB of perforin-dependent and perforin-independent (anoikis) apoptosis, inflammation derived by the activation of some cytokines belonging to the IL-1 cytokine family, ECM remodeling, epithelial-to-mesenchymal transition (EMT) and fibrosis. A greater comprehension of the pathophysiological consequences of GrB-mediated multiple activities may favor the design of new therapies aim to inhibit different inflammatory pathological conditions such as inflammaging and age-related diseases, EMT and organ fibrosis.

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The role of decorin in cardiovascular diseases: more than just a decoration

Cited by 26 publications

References 88 publications

Proteoglycans in Obesity-Associated Metabolic Dysfunction and Meta-Inflammation

Proteoglycans in Obesity-Associated Metabolic Dysfunction and Meta-Inflammation

Quantitative proteomics reveal the alterations in the spinal�cord after myocardial ischemia‑reperfusion injury in rats

Granzyme B in Inflammatory Diseases: Apoptosis, Inflammation, Extracellular Matrix Remodeling, Epithelial-to-Mesenchymal Transition and Fibrosis

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